Notoginsenoside R1 attenuates amyloid-β-induced damage in neurons by inhibiting reactive oxygen species and modulating MAPK activation.

Abstract Progressive accumulation of amyloid-β (Aβ) is a pathological hallmark of Alzheimer's disease (AD). Aβ increases free radical production in neuronal cells, leading to oxidative stress and cell death. An intervention that would reduce Aβ-related neurotoxicity through free radical reduction could advance the treatment of AD. Notoginsenoside R1 (NR1), the major and most active ingredient in the herb Panax notoginseng , can reduce reactive oxygen species and confer some neuroprotective effects. Here, NR1 was applied in a cell-based model of Alzheimer's disease. Cell viability, cell death, reactive oxygen species generation, and mitochondrial membrane potential were assessed in cultured PC12 neuronal cells incubated with Aβ 25–35 . In this model, Aβ was neurotoxic and induced necrosis and apoptosis; however, NR1 significantly counteracted the effects of Aβ by increasing cell viability, reducing oxidative damage (including apoptosis), restoring mitochondrial membrane potential, and suppressing stress-activated MAPK signaling pathways. These results promise a great potential agent for Alzheimer's disease and other Aβ pathology-related neuronal degenerative disease.